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• W2109471960 endingPage "1056" @default.
• W2109471960 startingPage "1049" @default.
• W2109471960 abstract "The histamine H2 receptor (H2r) belongs to the heptahelical receptor family; upon agonist binding, members of this family activate a G protein and the downstream effector adenylyl cyclase. Like other G protein-coupled receptors, exposure of H2r to agonists produces a desensitization of the response. The present study focused on the desensitization mechanism of this receptor. Using transiently transfected COS-7 cells expressing tagged-H2r, the desensitization induced by amthamine, characterized by decreased cAMP production, was studied. Results show that the receptor was rapidly desensitized with a t(1/2) = 0.49 +/- 0.01 min. Because of the rapid nature of H2r desensitization, receptor phosphorylation was examined as a likely mechanism for signal attenuation. H2r desensitization was not affected by protein kinases A and C (PKA and PKC) inhibitors but was remarkably reduced by Zn(2+), an inhibitor of G protein-coupled receptor kinases (GRKs). Cotransfection experiments using tagged H2r and different GRKs (2, 3, 5, or 6), demonstrated that GRK2 and GRK3 were the most potent in augmenting desensitization, causing a reduction in the maximal response to amthamine and a decrease of the t(1/2) for desensitization, whereas GRK5 and GRK6 did not affect the signaling. Receptor phosphorylation correlates with desensitization for each GRK studied, whereas phosphorylation that is dependent on protein kinases A and C seemed irrelevant in receptor signal termination. These results indicate that in H2r-transfected COS-7 cells, exposure to an agonist caused desensitization controlled by H2r phosphorylation via GRK2 and GRK3." @default.
• W2109471960 created "2016-06-24" @default.
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• W2109471960 date "2001-11-01" @default.
• W2109471960 modified "2023-09-27" @default.
• W2109471960 title "Histamine H2 Receptor Desensitization: Involvement of a Select Array of G Protein-Coupled Receptor Kinases" @default.
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• W2109471960 doi "https://doi.org/10.1124/mol.60.5.1049" @default.
• W2109471960 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11641433" @default.
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